Hyperin inhibits nuclear factor kappa B and activates nuclear factor E2-related factor-2 signaling pathways in cisplatin-induced acute kidney injury in mice

Chao, Che‐Yi; Tsai, Chien‐Sung; Chang, Yee-Phoung; Chen, Jianming; Chin, Hong-Chan; Yang, Shyh‐Chyun

doi:10.1016/j.intimp.2016.09.020

Cited by 33 publications

(17 citation statements)

References 31 publications

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“…It is reported that hyperin could protect against hepatotoxin-induced liver diseases 16,17 . In addition, hyperin has been demonstrated to prevent cisplatin-induced renal damage in mice 19 . The present results demonstrated the protection of hyperin against cisplatin-induced liver injury.…”

Section: ■ Discussionmentioning

confidence: 99%

“…Male ICR mice (body weight [18][19][20][21][22] aspartate aminotransferase (ALT/AST), gamma glutamyl transferase (GGT) activities were determined with commercial kits according to the instructions of manufacturer.…”

Section: ■ Methodsmentioning

confidence: 99%

“…Furthermore, hyperin induces apoptosis in cancer cell and sensitizes it to cisplatin treatment 18 . It has also been demonstrated that hyperin protects against cisplatin-induced acute kidney injury in mice 19 . However, the effect of hyperin in hepatoprotection during cisplatin administration has not been reported so far.…”

Section: ■ Introductionmentioning

confidence: 97%

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Hyperin protects against cisplatin-induced liver injury in mice

Niu

Han

et al. 2017

Acta Cir. Bras.

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Purpose: To evaluate the effect of hyperin in cisplatin-induced liver injury in mice. Methods: Mice were pretreated with hyperin at doses of 25 mg/kg and 50 mg/kg, respectively, for six days, and intraperitoneal injection of cisplatin (40 mg/kg) was administrated one hour after the final intragastrication of hyperin. Twenty-four hours later, blood and liver were collected for further research. Results: A single injection of cisplatin (40 mg/kg) for 24 h significantly increased serum alanine and aspartate aminotransferases (ALT/AST) and gamma glutamyl transferase (GGT) activities, whileas hyperin reversed cisplatin-induced such increases. Liver histopathological examination further demonstrated the protection of hyperin against cisplatin-induced liver injury. Further results showed hyperin reversed cisplatin-induced the increase in content of malondialdehyde (MDA) and the decrease in level of total antioxidant capacity (T-AOC) in liver. Moreover, hyperin increased the levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), glutathione-s transferase (GST) in cisplatininduced liver. Conclusion: Hyperin inhibits cisplatin-induced hepatic oxidative stress, which contributes greatly to the amelioration of cisplatin-induced liver injury in mice.

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Section: ■ Discussionmentioning

confidence: 99%

Section: ■ Methodsmentioning

confidence: 99%

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Hyperin protects against cisplatin-induced liver injury in mice

Niu

Han

et al. 2017

Acta Cir. Bras.

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“…Several flavonoids attenuate cisplatin-induced renal injury in rats and mice, mitigating cisplatin-induced histopathologic alterations and reducing the increases in serum creatinine and blood urea nitrogen. Their mechanism of action involves several pathways of the inflammatory cascade and oxidative perturbations (Tanabe et al, 2012 ; Malik et al, 2015 , 2016 ; Arab et al, 2016 ; Chao et al, 2016 ; He et al, 2016 ; Hassan et al, 2017 ; Huang D. et al, 2017 ; Huang Y. C. et al, 2017 ; Lee et al, 2017 ; Ma et al, 2017 ), including: the downregulation of activated NF-κB p65 protein expression and its downstream effectors (e.g., iNOS and TNF-α), with restoration of the anti-inflammatory IL-10; and reductions in phospho-NF-κB p65 and phospho-P38 MAPK activation and Nrf2 expression in cisplatin-induced renal injury. Flavonoids also downregulated the expression of the apoptotic marker caspase-3, inhibiting cisplatin-induced apoptosis and thereby favoring renal cell survival.…”

Section: Nephrotoxic Agentsmentioning

confidence: 99%

Flavonoids in Kidney Health and Disease

et al. 2018

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This review summarizes the latest advances in knowledge on the effects of flavonoids on renal function in health and disease. Flavonoids have antihypertensive, antidiabetic, and antiinflammatory effects, among other therapeutic activities. Many of them also exert renoprotective actions that may be of interest in diseases such as glomerulonephritis, diabetic nephropathy, and chemically-induced kidney insufficiency. They affect several renal factors that promote diuresis and natriuresis, which may contribute to their well-known antihypertensive effect. Flavonoids prevent or attenuate the renal injury associated with arterial hypertension, both by decreasing blood pressure and by acting directly on the renal parenchyma. These outcomes derive from their interference with multiple signaling pathways known to produce renal injury and are independent of their blood pressure-lowering effects. Oral administration of flavonoids prevents or ameliorates adverse effects on the kidney of elevated fructose consumption, high fat diet, and types I and 2 diabetes. These compounds attenuate the hyperglycemia-disrupted renal endothelial barrier function, urinary microalbumin excretion, and glomerular hyperfiltration that results from a reduction of podocyte injury, a determinant factor for albuminuria in diabetic nephropathy. Several flavonoids have shown renal protective effects against many nephrotoxic agents that frequently cause acute kidney injury (AKI) or chronic kidney disease (CKD), such as LPS, gentamycin, alcohol, nicotine, lead or cadmium. Flavonoids also improve cisplatin- or methotrexate-induced renal damage, demonstrating important actions in chemotherapy, anticancer and renoprotective effects. A beneficial prophylactic effect of flavonoids has been also observed against AKI induced by surgical procedures such as ischemia/reperfusion (I/R) or cardiopulmonary bypass. In several murine models of CKD, impaired kidney function was significantly improved by the administration of flavonoids from different sources, alone or in combination with stem cells. In humans, cocoa flavanols were found to have vasculoprotective effects in patients on hemodialysis. Moreover, flavonoids develop antitumor activity against renal carcinoma cells with no toxic effects on normal cells, suggesting a potential therapeutic role in patients with renal carcinoma.

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“…Adenosine 5′-monophosphate-activated protein kinase (AMPK) is a crucial kinase involved in maintaining cellular energy homeostasis. Silent information regulator T1 (Sirt1), a NAD + -dependent histone deacetylase, plays diverse roles in stress resistance, apoptosis, senescence, aging, and inflammation [11]. Evolving data have suggested that the AMPK/Sirt1 pathway plays an important role in renal inflammation and can act as a therapeutic target for inflammationassociated diseases [12].…”

Section: Introductionmentioning

confidence: 99%

Cordyceps cicadae Mycelia Ameliorate Cisplatin-Induced Acute Kidney Injury by Suppressing the TLR4/NF-κB/MAPK and Activating the HO-1/Nrf2 and Sirt-1/AMPK Pathways in Mice

Deng

Jiang

Chen

et al. 2020

Oxidative Medicine and Cellular Longevity

100

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Acute kidney injury (AKI) is a common clinical problem, characterized by a sudden loss of renal function, a high risk of death, and the eventual development of renal fibrosis and renal failure. Cordyceps cicadae is a traditional Chinese medicine with the potential function of kidney protection. We analyze two sputum extracts, a water extract (WCC), and an ethanol extract (ECC), to assess the potential of treating AKI in an animal model of kidney injury induced by cisplatin. A nephrotoxic mouse model was first established by intraperitoneal injection of cisplatin. Subsequently, WCC and ECC were orally administered in these mice. The results show that WCC and ECC significantly alleviated cisplatin-induced AKI renal histological changes, serum creatinine (CRE) and blood urea nitrogen (BUN) production, and the levels of NO, TNF-α, IL-1β, and IL-6. The levels of malondialdehyde (MDA) and glutathione (GSH) were suppressed by administration of WCC and ECC. However, WCC treatment prevented these changes significantly better than ECC treatment. In addition, Western blot data showed that WCC attenuated the cisplatin-induced protein expression of cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS), as well as inhibiting nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) activation in the kidney tissues. Furthermore, WCC greatly inhibited the expression of Toll-like receptor 4 (TLR4) and cisplatin-induced NF-κB activation, as well as dramatically increasing the production of antioxidative enzymes (i.e., superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase 1 (HO-1)), silent information regulator T1 (Sirt1), and p-AMP-activated protein kinase (AMPK) in the kidney tissues. In addition, we found that WCC increased the expression levels of the autophagy-related proteins LC3B and Beclin-1; proapoptotic proteins, including cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase (PARP) 1; and organic anion transporters 1 (OAT1) and 3 (OAT3) in the kidney tissues. Finally, WCC, ECC, and two bioactive compounds—adenosine and N6-(2-hydroxyethyl) adenosine (HEA)—inhibited the production of nitrite oxide (NO) and intracellular reactive oxygen species (ROS) triggered by lipopolysaccharide- (LPS-) stimulated RAW264.7 macrophages in vitro. Collectively, WCC could provide a potential therapeutic candidate for the prevention of cisplatin-induced kidney injury through the inhibition of oxidative stress and inflammation.

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Hyperin inhibits nuclear factor kappa B and activates nuclear factor E2-related factor-2 signaling pathways in cisplatin-induced acute kidney injury in mice

Cited by 33 publications

References 31 publications

Hyperin protects against cisplatin-induced liver injury in mice

Hyperin protects against cisplatin-induced liver injury in mice

Flavonoids in Kidney Health and Disease

Cordyceps cicadae Mycelia Ameliorate Cisplatin-Induced Acute Kidney Injury by Suppressing the TLR4/NF-κB/MAPK and Activating the HO-1/Nrf2 and Sirt-1/AMPK Pathways in Mice

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